Implantable cardiac stimulation devices are well known in the art. They include implantable pacemakers which provide stimulation pulses to cause a heart, which would normally beat too slowly or at an irregular rate, to beat at a controlled normal rate. They also include defibrillators, which detect when the atria and/or the ventricles of the heart are in fibrillation or a pathologic rapid organized rhythm and apply cardioverting or defibrillating electrical energy to the heart to restore the heart to a normal rhythm. Implantable cardiac stimulation devices may also include the combined functions of a pacemaker and a defibrillator.
As is well known, implantable cardiac stimulation devices sense cardiac activity for monitoring the cardiac condition of the patient in which the device is implanted. By sensing the cardiac activity of the patient, the device is able to provide cardiac stimulation pulses when they are needed and inhibit the delivery of cardiac stimulation pulses at other times. This inhibition accomplishes two primary functions. Firstly, when the heart is intrinsically stimulated, its hemodynamics are often improved. Secondly, inhibiting the delivery of a cardiac stimulation pulse reduces the battery current drain on that cycle and extends the life of the battery, which powers and is located within the implantable cardiac stimulation device. Extending the battery life will therefore delay the need to explant and replace the cardiac stimulation device due to an expended battery. Generally, the circuitry used in implantable cardiac stimulation devices have been significantly improved since their introduction such that the major limitation of the battery life is primarily the number and amplitude of the pulses being delivered to a patient's heart. Accordingly, it is preferable to minimize the number of pulses delivered by using this inhibition function and to minimize the amplitude of the pulses where this is clinically appropriate.
It is well known that the amplitude value of a pulse that will reliably stimulate a patient's heart, i.e., its threshold value, will change over time after implantation and will vary with the patient's activity level and other physiological factors. To accommodate for these changes, pacemakers may be programmed to deliver a pulse at an amplitude well above (by an increment or a factor) an observed threshold value. To avoid wasting battery energy, an automatic capture/threshold capability was developed to automatically adjust the pulse amplitude to accommodate for these long and short-term physiological changes. In an existing device, the Affinity™ DR, Model 5330 L/R Dual-Chamber Pulse Generator, manufactured by the assignee of the present invention, an AUTOCAPTURE™ pacing system is provided. The User's Manual, ©1998 St. Jude Medical, which describes this capability, is incorporated herein by reference in its entirety. In this system, the threshold level is automatically determined in a threshold search routine and is maintained by a capture verification routine. Once the threshold search routine has determined a pulse amplitude that will reliably stimulate, i.e., capture, the patient's heart, the capture verification routine monitors signals from the patient's heart to identify pulses that do not stimulate the patient's heart (indicating a loss-of-capture). Should a loss-of-capture (LOC) occur, the capture verification routine will generate a large amplitude (e.g., 4.5 volt) backup pulse shortly after (typically within 80–100 ms) the original (primary) stimulation pulse. This capture verification occurs on a pulse-by-pulse basis and thus, the patient's heart will not miss a beat.
In order to determine the threshold level, the automatic capture routine periodically (e.g., every 8 hours or according to a loss-of-capture criteria) shortens the programmed AV/PV delays. Shortening of the AV/PV (atrial stimulation pulse to ventricular stimulation pulse or intrinsic P-wave to ventricular stimulation pulse) delays guarantees that conduction of an atrial event (e.g., an atrial stimulation pulse (A-pulse) or P-wave) via the AV node to the ventricle will not contribute to a ventricular event. That is, an evoked response and an R-wave will not combine and result in a fusion beat. Typically, the AV/PV delays are respectively shortened to 50 and 25 ms (milliseconds). Accordingly, when a ventricular stimulation pulse (V-pulse) is delivered, any response in the ventricle can be treated as an evoked response to the primary V-pulse and a lack of response will indicate that the V-pulse amplitude level is below the threshold value for stimulating the ventricle. However, this shortened AV/PV delay is likely to be hemodynamically suboptimal and may create patient discomfort or possibly even cause an elevation in heart rate or AV nodal conduction time through modified ANS tone, baroreflex, or release of endogenous catecholamines. All of these may influence the results of the automatic threshold determination. In one case, since the evoked response morphology is correlated with heart rate and myocardial conduction velocity, automatically setting the evoked response sensitivity level based upon evoked responses measured from “excited” myocardium may allow a higher evoked response sense level to be set for automatic capture detection. Then, when a basal myocardial state is achieved, false losses-of-capture may be more frequent. Additionally, it is well known that elevated sympathetic tone can reduce capture thresholds. If a short AV/PV delay causes an increase in sympathetic tone or released catecholamines, then the capture threshold values determined using the short AV/PV delay may cause the pacing output energy to be set at or below the threshold found at more basal myocardial states. This would result in more “unnecessary” and possibly uncomfortable threshold searches.
Furthermore, while the predetermined, e.g., 50/25 ms, selection is suitable for the vast majority of patients, some patients, e.g., those with first degree heart block, do not require as large a decrease during automatic capture determination and other patients, e.g., those with complete heart block, may not require any AV/PV delay decrease during automatic capture determination. In such patients, a fixed shortening of the AV/PV delays can unnecessarily cause patient discomfort.
Therefore what is needed is a flexible system that can optimize AV/PV delay settings used for automatically determining a threshold amplitude value for the primary ventricular stimulation pulse wherein the optimized AV/PV delays are determined for the individual patient to minimize any adverse hemodynamic effects during the automatic threshold determination.